Einfluss von Makrophagen und IL-6 auf die axonale Regeneration bei der adulten Ratte
Auch gedruckt in der BibliothekZ: J-H 13.042; W: W-H 11.496
FakultätenFakultät für Naturwissenschaften
LizenzStandard (Fassung vom 01.10.2008)
Retinal ganglion cells (RGCs) cannot regenerate their axons after injury and undergo apoptosis soon after an intraorbital injury of the optic nerve. However, RGCs reactivate their axonal growth program when inflammatory reactions occur in the eye. This enables them to survive axotomy and to regenerate lengthy axons into the lesioned optic nerve. Lens injury and zymosan injections can induce these beneficial progresses and provoke also a strong accumulation of the activated macrophages in the vitreous body. It has recently been suggested that macrophage-derived oncomodulin is the principal mediator of this phenomenon. I show here that oncomodulin is not significantly expressed in primary macrophages and that the intraocular levels of this protein do not increase after lens injury or zymosan treatment. Furthermore, greatly reducing the invasion of macrophages into the inner eye does not diminish the neuroprotective effects of lens injury, but rather increases axon regeneration into the optic nerve. Axon regeneration is correlated with the activation of retinal astrocytes and Müller cells. This data suggest that intraocular inflammation mediates its main beneficial effects through factors other than oncomodulin and that the underlying mechanism might be independent of the presence of activated macrophages. I show here that lens injury induce upregulation of IL-6 into the inner eye. Intravitreally applied IL-6 allow RGCs to regenerate axons in the injured optic nerve. This data suggest that IL-6 is a contributor to the axon-growth-promoting effects of lens injury.
Erstellung / Fertigstellung
Normierte SchlagwörterInterleukin 6 [GND]